Both species, oAβ and fAβ, stimulate the activation of microglia in the AD brain, leading to a proinflammatory response mediated by cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), in addition to the complement system and chemokines. Here, IL1B is linked to Alzheimer disease.